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Mutant huntingtin binds the mitochondrial fission GTPase dynamin-related protein-1 and increases its enzymatic activity

Huntington's disease is characterized by mitochondrial dysfunction and neuron death. Now, Ella Bossy-Wetzel and her colleagues report that the aberrant interaction of mutant huntingtin protein with the mitochondrial fission protein DRP1 results in DRP1 activation. Blocking DRP1 activity can reduce mutant huntingtin–induced cell death.

Wenjun Song
Jin Chen
Ella Bossy-Wetzel
Research20 Feb 2011
Nature Medicine

Volume: 17, P: 377-382
Mitochondrial fragmentation in neurodegeneration

There is mounting evidence that mitochondrial dysfunction is an early and causal event in neurodegeneration. Here, Bossy-Wetzel and colleagues discuss how aberrant mitochondrial fission and fusion can contribute to neurodegenerative disease.

Andrew B. Knott
Guy Perkins
Ella Bossy-Wetzel
Reviews01 Jul 2008
Nature Reviews Neuroscience

Volume: 9, P: 505-518
Molecular pathways to neurodegeneration

Ella Bossy-Wetzel
Robert Schwarzenbacher
Stuart A Lipton
Reviews01 Jul 2004
Nature Medicine

Volume: 10, P: S2-S9
Cerium oxide nanoparticles protect against Aβ-induced mitochondrial fragmentation and neuronal cell death

J M Dowding
W Song
E Bossy-Wetzel
Research06 Jun 2014
Cell Death & Differentiation

Volume: 21, P: 1622-1632
Primary cilia and autophagic dysfunction in Huntington’s disease

M Kaliszewski
A B Knott
E Bossy-Wetzel
Reviews10 Jul 2015
Cell Death & Differentiation

Volume: 22, P: 1413-1424

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Mutant huntingtin binds the mitochondrial fission GTPase dynamin-related protein-1 and increases its enzymatic activity

Mitochondrial fragmentation in neurodegeneration

Molecular pathways to neurodegeneration

Cerium oxide nanoparticles protect against Aβ-induced mitochondrial fragmentation and neuronal cell death

Primary cilia and autophagic dysfunction in Huntington’s disease

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